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PathY5 > Respiratory Histopathology > Flashcards

Respiratory Histopathology Flashcards

1
Q

What does VITAMIN CDEF stand for?

A

Vascular
Infective/ Inflammatory
Trauma
Autoimmune
Metabolic
Iatrogenic
Neoplastic

Congenital
Degenerative
Endocrine/ environment
Functional

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2
Q

What are the important lung diseases you need to know?

A

COPD
Asthma
Chronic bronchitis
Respiratory failure
Pneumonia
Tuberculosis
Bronchiectasis
Cystic fibrosis

Lung cancer
Mesothelioma

URTI
Carcinoma of the larynx

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3
Q

What is pulmonary oedema?

A

Accumulation of fluid in alveolar spaces as consequence of “leaky capillaries” or “backpressure” from failing left ventricle

Poor gas exchange = hypoxia = respiratory failure

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4
Q

Summarise the important parts of pulmonary oedema

A

Often associated with heart failure (acute or chronic).

Very common cause of acute and chronic respiratory failure in A&E and community, and common finding at post mortem.

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5
Q

What are the causes of pulmonary oedema?

A

Left heart failure
Alveolar injury (drugs, inhalation, infection, pancreatitis)
Neurogenic - head injury
High altitude- altitude sickness

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6
Q

What is the pathology of pulmonary oedema?

A

Acute: Heavy watery lungs, intra-alveolar fluid on histology

Chronic: Iron laden macrophages, fibrosis

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7
Q

What causes ARDS in adults?

A

V- Blood transfusion, DIC, Shock

I- Infection (local or generalised sepsis), Pancreatitis

T- Aspiration, Trauma, Inhaled irritant gases

M- Drug overdose

Idiopathic

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8
Q

What causes hyaline membrane disease of newborn?

A

Insufficient surfactant production
Premature babies

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9
Q

What is Acute lung injury pattern/Diffuse alveolar damage?

A

Important cause of rapid onset respiratory failure – difficult to treat, patients end up on ICU

Caused by acute damage to endothelium and/or alveolar epithelium

Basic pathology is the same in all = Diffuse alveolar damage

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10
Q

What does diffuse alveolar damage cause?

A

Lungs are expanded and firm

Plum coloured, airless

Often weigh >1kg

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11
Q

What is the outcome of diffuse alveolar damage?

A

Death ~ 40%
Superimposed infection
Resolution : Lung returns to normal
Residual fibrous scarring of lung : Chronic respiratory impairment

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12
Q

Summarise the definition, epidemiology and presentation of asthma

A

Chronic inflammatory airway disorder with recurrent episodes widespread narrowing of the airways that changes in severity over short periods of time.

Prevalence increased in recent decades >10% children, 5% adults

Presents with wheezing, chest tightness, SOB, night-time cough
In a severe attack patients develop status asthmaticus.

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13
Q

What are the causes of asthma?

A

Atopic: genetic tendency to develop allergic reaction to common environmental allergen (e.g. house dust mites)

Non-atopic
Air pollution
Drugs - NSAIDs
Occupational – inhaled gases/fumes
Diet
Genetic factors
Physical exertion – “cold”
Intrinsic

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14
Q

What are the acute and chronic changes of asthma?

A

Acute change
Bronchospasm, oedema, hyperaemia, inflammation

Chronic change
Muscular hypertrophy
Airway narrowing
Mucus plugging

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15
Q

How does COPD present?

A

Very common cause chronic respiratory failure. May present with acute (often infective) exacerbations

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16
Q

What causes COPD?

A

~80% are smokers

Smoking causes inflammation and secondary damage to airways and interstitium

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17
Q

What is he pathology of COPD?

A

Mix of airway and alveolar pathology (chronic bronchitis and emphysema), resulting in progressive airway obstruction

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18
Q

What is chronic bronchitis?

A 
Chronic cough (and inflammation) productive of sputum 
Most days for at least 3 months over at least 2 consecutive years
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19
Q

What is the pathology of chronic bronchitis?

A

Dilated airways
Mucus gland hyperplasia
Goblet cell hyperplasia
Mild inflammation

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20
Q

What are the complications of COPD/ chronic bronchitis?

A

Infections
Respiratory failure
Pulmonary HTN
Right sided HF
Lung Cancer

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21
Q

What is emphysema?

A

A permanent loss of the alveolar parenchyma distal to the terminal bronchiole

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22
Q

What is the pathophysiology of emphysema?

A

Cigarette smoking causes reduced Alpha 1 antitrypsin and other antiproteases as well as inflammation (neutrophil and macrophage activation)

This increases proteases in the lung which causes tissue damage

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23
Q

What is the histological difference between smoking and alpha 1 antitrypsin deficiency?

A

Smoking- Loss centred on bronchiole - CENTRILOBULAR

Alpha 1 antitrypsin deficiency- Diffuse loss of alveolae - PANACINAR

24
Q

What are the complications of emphysema?

A

Large air spaces (bullae)
Rupture - pneumothorax

Respiratory failure

Pulmonary hypertension and right sided heart failure.

25
Q

What is bronchiectasis?

A

Permanent abnormal dilatation of bronchi with inflammation and fibrosis extending into adjacent parenchyma

26
Q

Where does bronchiectasis occur?

A

Variation in site depending on cause (idiopathic often involves lower lobe)

27
Q

What does bronchiectasis cause?

A

Inflamed scarred lungs with dilated airways

28
Q

What are the causes and associations of bronchiectasis?

A

Inflammatory
Congenital

29
Q

What are the inflammation related causes of bronchiectasis?

A
  1. Infection
    • Post-infectious (especially children or cystic fibrosis)
    • Abnormal host defense 1º [hypogammagl.] and 2º [chemotherapy, NG]
    • Ciliary dyskinesia 1º [Kartagener’s] and 2º
  2. Obstruction (extrinsic/intrinsic/middle lobe syn.)
  3. Post-inflammatory (aspiration)
  4. Secondary to bronchiolar disease (OB) and interstitial fibrosis (CFA, sarcoidosis)
  5. Systemic disease (connective tissue disorders)
  6. Asthma
30
Q

What are the complications of bronchiectasis?

A

Recurrent infections
Haemoptysis
Pulmonary Hypertension and right sided heart failure
Amyloidosis

31
Q

What is cystic fibrosis epidemiology?

A

Affects 1 in 2,500 live births

Autosomal recessive (approx 1/20 of population are heterozygous carriers)

Chr 7q3 = CFTR gene (Cystic Fibrosis Transmembrane Conductance Regulator) = chloride ion transporter protein. >1400 mutations, but commonest Delta F508

32
Q

What is cystic fibrosis?

A

Abnormality leads to defective ion transport across cell membranes leading to excessive resorption of water from secretions of exocrine glands.

33
Q

What is affected in CF?

A

Generalised disease of exocrine glands resulting in abnormally thick mucus secretion - affects all organ systems.
GI tract -> meconium ileus, malabsorption
Pancreas -> pancreatitis, malabsorption
Liver -> cirrhosis
Male reproductive system -> infertility

Lung

34
Q

What lung infections do you get in CF?

A

Over 90% of patients have lung involvement:

  • Recurrent infections (P.aeruginosa, S.aureus, H. influenzae, B.cepacia)
  • Haemoptysis, Pneumothorax, Chronic respiratory failure and cor pulmonale, Allergic bronchopulmonary aspergillosis (ABPA), Atelectasis, BRONCHIECTASIS
35
Q

How do you treat CF?

A

Improved treatment (physio, antibiotics, enzyme supplements /creon/, parenteral nutrition) has led to survival often into fourth decade

Lung transplantation offers longer survival

36
Q

What can cause pulmonary infections?

A

Bacterial, including mycobacteria
Viral
Mycoplasma
Fungal & parasitic – think if history of foreign travel
Opportunistic infections (CMV, Pneumocystis, fungal) - think if history of immunosuppression

37
Q

What are the symptoms of pulmonary infections?

A

Shortness of breath, cough, fever, purulent sputum

38
Q

What are the most common organisms that cause pulmonary infections in:

  • The community
  • Hospital
  • Aspiration
A

Community acquired: streptococcus pneumoniae, haemophilis influenzae, mycoplasma
Hospital acquired: gram –ve (klebsiella, pseudomonas)
Aspiration: Mixed aerobic and anaerobic

39
Q

What are the patterns of pulmonary infections?

A

Bronchopneumonia
Lobar pneumonia
Abscess formation
Granulomatous inflammation

40
Q

What is bronchopneumonia pathology?

A

Pathology - Patchy bronchial and peribronchial distribution, often lower lobes

41
Q

When does bronchopneumonia happen?

A

Compromised host defense - Elderly

Often low virulence organisms - Staphylococcus, Haemophilius, Streptococcus, Pneumococcus,

42
Q

What is the histopathology in bronchopneumonia?

A

Peribronchial distribution

Acute inflammation surrounding airways and within alveoli

43
Q

What is and what causes lobar pneumonia?

A

Acute bacterial infection of a large portion of a lobe or entire lobe.
Infrequent with advent of antibiotics
90-95% pneumococci (S. pneumoniae)
Widespread fibrinosuppurative consolidation

44
Q

What is the histopathology of lobar pneumonia?

A
  1. Congestion
    Hyperaemia
    Intra-alveolar fluid
  2. Red hepatization
    Hyperaemia
    Intra-alveolar neutrophils
  3. Grey hepatization
    Intra-alveolar connective tissue
  4. Resolution
    Restoration normal architecture.
45
Q

What are complications of lung infection?

A

Abscess formation
Pleuritis and pleural effusion
Infected pleural effusion (EMPYEMA)
Fibrous scarring
Septicaemia

46
Q

What is a granuloma?

A

Collection of histiocytes/macrophages +/- multinucleate giant cells
Necrotising or non necrotising

47
Q

What causes caseating granulomas?

A

TB- Fairly common in urban community and immunosuppressed.

Other causes include fungi and parasites
History of foreign travel

48
Q

What causes atypical pneumonia?

A

Mycoplasma, viruses (e.g. CMV, influenza), Coxiella, Chlamydia

49
Q

What is the result of atypical pneumonia?

A

Interstitial inflammation (pneumonitis) without accumulation of intra-alveolar inflammatory cells

Chronic inflammatory cells within alveolar septa with oedema +/- viral inclusions

50
Q

What is a pulmonary thromboembolus?

A

Occlusion of pulmonary artery by thromboembolus

51
Q

What may occur just prior to a pulmonary embolus?

A

Common site formation in deep veins of leg (95%)
Present with swelling of leg (DVT)
Present with symptoms of spread to lung (pulmonary embolism)

52
Q

What is virchows triad in relation to PE?

A

factors promoting blood stasis
damage to endothelium
increased coagulation

53
Q

What are the RFs for a PE?

A

Advanced age, female sex, obesity, immobility, cardiac failure, malignancy, trauma, surgery, childbirth, haemoconcentration, polycythaemia, DIC, contraceptive pill, cannulation, anti-phospholipid syndrome.

54
Q

What are the effects of a PE based on size?

A

Small peripheral pulmonary arterial occlusion

Haemorrhagic infarct

Repeated emboli cause increasing occlusion of pulmonary vascular bed and pulmonary hypertension

Large emboli can occlude the main pulmonary trunk (saddle embolus)

Sudden death, acute right heart failure, or cardiovascular shock occurs in 5% of cases when >60% of pulmonary bed is occluded

55
Q

How may a patient present with PE?

A

Patients present with pleuritic chest pain or chronic progressive shortness of breath due to pulmonary hypertension

Sudden death, acute right heart failure, or cardiovascular shock occurs in 5% of cases when >60% of pulmonary bed is occluded

If patient survives, the embolus usually resolves

30% develop second or more emboli

56
Q

What causes a non thrombotic embolus?

A

Bone marrow
Amniotic fluid
Trophoblast
Tumour
Foreign body
Air

57
Q

What new disease exists in 2019?

A

Vaping associated acute lung injury

PathY5 (98 decks)

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